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Tubuloglomerular feedback responses in offspring of dexamethasone-treated ewes
Macquarie Univ, Fac Med & Hlth Sci, Sydney, NSW, Australia.;Univ New South Wales, Sch Med Sci, Dept Physiol, Sydney, NSW, Australia..
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology. Univ New South Wales, Sch Med Sci, Dept Physiol, Sydney, NSW, Australia.
Univ New South Wales, Sch Med Sci, Dept Physiol, Sydney, NSW, Australia..
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology. Univ New South Wales, Sch Med Sci, Dept Physiol, Sydney, NSW, Australia.
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2017 (English)In: American Journal of Physiology - Renal Physiology, ISSN 0363-6127, E-ISSN 1522-1466, Vol. 313, no 4, F864-F873 p.Article in journal (Refereed) Published
Abstract [en]

Via developmental programming, prenatal perturbations, such as exposure to glucocorticoids and maternal malnutrition alter kidney development and contribute to the development of hypertension. To examine the possibility that alterations in tubuloglomerular feedback (TGF) contribute to the development of hypertension in offspring following maternal dexamethasone treatment (Dex) in early gestation, studies were conducted in fetal sheep and lambs. Pregnant ewes were infused with dexamethasone (0.48 mg/h) at 26-28 days gestation. No differences were observed in mean arterial pressure, glomcrular.filtration rate. or electrolyte excretion rates between the.Dex and Untreated fetuses or lambs. Gestational exposure to Dex markedly enhanced TGF sensitivity, as the turning point in Dex treatedfetuses was significantly lower (12.9 +/- 0.9 nl/min; P < 0.05) compared with Untreated fetuses (17.0 +/- 1.0 til/min). This resetting of TOE sensitivity persisted after birth (P < 0.01). TGF reactivity did not differ between the groups in fetuses or lambs. In response to nitric oxide inhibition, TOE sensitivity increased (the turning point decreased) and reactivity increased in Untreated fetuses and lambs, but these effects were blunted in the Dex-treated fetuses and lambs. Our data suggest that an altered TOE response may be an underlying renal mechanism contributing to the development of hypertension in the Dex model of fetal programming. The lower tonic level of NO production in these dexamethasone-exposed offspring may contribute to the development of hypertension as adults.

Place, publisher, year, edition, pages
AMER PHYSIOLOGICAL SOC , 2017. Vol. 313, no 4, F864-F873 p.
Keyword [en]
tubuloglomerular feedback, fetal programming, dexamethasone
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-338533DOI: 10.1152/ajprenal.00538.2016ISI: 000412361700007PubMedID: 28679594OAI: oai:DiVA.org:uu-338533DiVA: diva2:1172439
Funder
Knut and Alice Wallenberg FoundationThe Swedish Foundation for International Cooperation in Research and Higher Education (STINT)
Available from: 2018-01-10 Created: 2018-01-10 Last updated: 2018-01-10Bibliographically approved

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Persson, Erik

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